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Myelin made by different cell types varies in chemical composition and configuration, but performs the same insulating function. Myelinated axons are white in appearance, hence the "white matter" of the brain.

The main purpose of a myelin layer (or sheath) is to increase in the speed at which impulses propagate along the myelinated fiber. Along unmyelinated fibers, impulses move continuously as waves, but, in myelinated fibers, they hop or "propagate by saltation." Myelin increases electrical resistance across the cell membrane by a factor of 5,000 and decreases capacitance by a factor of 50.[How to reference and link to summary or text] Thus, myelination helps prevent the electrical current from leaving the axon.

When a peripheral fiber is severed, the myelin sheath provides a track along which regrowth can occur. Unmyelinated fibers and myelinated axons of the mammalian central nervous system do not regenerate.

Research to repair damaged myelin sheaths is ongoing. Techniques include surgically implanting oligodendrocyte precursor cells in the central nervous system and inducing myelin repair with certain antibodies. While there have been some encouraging results in mice (via stem cell transplantation), it is still unknown whether this technique can be effective in replacing myelin loss in humans.[4]

Demyelination (i.e., the destruction or loss of the myelin sheath) results in diverse symptoms determined by the functions of the affected neurons. It disrupts signals between the brain and other parts of the body; symptoms differ from patient to patient, and have different presentations upon clinical observation and in laboratory studies.

Typical symptoms include:

blurriness in the central visual field that affects only one eye; may be accompanied by pain upon eye movement;

double vision;

odd sensation in legs, arms, chest, or face, such as tingling or numbness (neuropathy);

weakness of arms or legs;

cognitive disruption including speech impairment and memory loss;

heat sensitivity (symptoms worsen, reappear upon exposure to heat such as a hot shower);

Research to repair damaged myelin sheaths is ongoing. Techniques include surgically implanting oligodendrocyte precursor cells in the central nervous system and inducing myelin repair with certain antibodies. While results in mice have been encouraging (via stem cell transplantation), whether this technique can be effective in replacing myelin loss in humans is still unknown.[8]Cholinergic treatments, such as acetylcholinesterase inhibitors (AChEIs), may have beneficial effects on myelination, myelin repair, and myelin integrity. Increasing cholinergic stimulation also may act through subtle trophic effects on brain developmental processes and particularly on oligodendrocytes and the lifelong myelination process they support. By increasing oligodendrocyte cholinergic stimulation, AChEIs, and other cholinergic treatments, such as nicotine, possibly could promote myelination during development and myelin repair in older age.[9]
Glycogen synthase kinase 3β inhibitors such as Lithium Chloride have been found to promote myelination in mice with damaged facial nerves[10]

Donaldson, H.H. & Hoke, G.W. (1905). "The areas of the axis cylinder and medullary sheath as seen in cross sections of the spinal nerves of vertebrates". Journal of Comparative Neurology. 15, 1- — [Early evidence of approximately-constant ratio of myelin-thickness to axon diameter].

Traill, R.R. (1977/1980/2006) Toward a theoretical explanation of electro-chemical interaction in memory-use. Monograph #24, Cybernetics Department, Brunel University.[4], or as Part B of Thesis.[5] — [showing that other extra signal-modes are possible for such "coaxials", which could make myelin even more important].

Traill, R.R. (1988). "The case that mammalian intelligence is based on sub-molecular memory-coding and fibre-optic capabilities of myelinated nerve axons". Speculations in Science and Technology. 11(3), 173-181.